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Remifentanil regulates proliferation and apoptosis of gastric cancer cells by regulating miR-206/GOLPH3
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- Author:
- No author available
- Journal Title:
- World Chinese Journal of Digestology
- Issue:
- 4
- DOI:
- 10.11569/wcjd.v27.i4.228
- Key Word:
- 瑞芬太尼;胃癌;miR-206;GOLPH3
Abstract： 背景 瑞芬太尼为临床上常用的麻醉药,近几年其新功效不断被发现,尤其是抗癌功能.但瑞芬太尼在胃癌(gastric cancer,GC)中的作用及机制尚未清楚.目的 探讨瑞芬太尼对AGS、MKN-45人GC细胞中miR-206、GOLPH3表达及细胞增殖、凋亡的影响.方法 以40 nmol/L瑞芬太尼干预AGS、MKN-45细胞,qRT-PCR、Western blot、MTT和流式细胞仪分别检测细胞中miR-206和GOLPH3表达及细胞活力、凋亡.在AGS、MKN-45细胞中过表达miR-206或敲减GOLPH3,MTT和流式细胞仪检测细胞活力和凋亡.Targetscan在线预测、双荧光素酶报告基因实验和Western blot实验验证miR-206和GOLPH3的靶向关系.将miR-206 inhibitors或pcDNA-GOLPH3转染至AGS、MKN-45细胞并以40 nmol/L瑞芬太尼进行处理,检测细胞活力和凋亡.结果 瑞芬太尼干预的AGS、MKN-45细胞中miR-206高表达而GOLPH3低表达,细胞活力降低而凋亡率升高.过表达miR-206或敲减GOLPH3,细胞活力下降、凋亡率升高.Targetscan在线预测、双荧光素酶报告基因实验和Western blot实验结果表明,miR-206可靶向调控GOLPH3蛋白表达.下调miR-206或过表达GOLPH3能够逆转瑞芬太尼对AGS、MKN-45细胞增殖的抑制和凋亡的促进作用.结论 瑞芬太尼能够通过调节miR-206和GOLPH3表达抑制AGS、MKN-45细胞增殖并诱导凋亡.
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